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1.
Clinics (Sao Paulo) ; 71(4): 226-31, 2016 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-27166774

RESUMO

OBJECTIVES: To establish cut-off values for growth hormone concentrations using clonidine as a secretagogue and an immunochemiluminescent assay as the method of measurement and to analyze the response time as well as the influence of gender, nutritional status and pubertal stage. METHODS: A total of 225 tests were performed in 3 patient groups, categorized as group 1 (normal), group 2 (idiopathic short stature) and group 3 (growth hormone deficiency). Among the 199 disease-free individuals, 138 were prepubertal, and 61 were pubertal. Clonidine (0.1 mg/m2) was orally administered, and the growth hormone level was measured by immunochemiluminescent assay. The growth hormone peak and the difference between the growth hormone peak and the baseline level were then analyzed. Statistical analyses were performed using Student's t-test or the Mann-Whitney test and Kruskal-Wallis test followed by Dunn's post hoc test. Cut-off values were determined using a receiver operating characteristic curve. RESULTS: Group 1 and group 2 had no difference in growth hormone peak, gender, body mass index standard deviation score, or pubertal stage. Group 3 exhibited a significantly lower growth hormone peak than the other groups did. The receiver operating characteristic curve demonstrated that growth hormone concentrations ≥ 3.0 ng/mL defined responsiveness to clonidine. In total, 3.02% of individuals in group 1 and group 2 were considered false positive, i.e., these children lacked growth hormone deficiency and had a peak below 3.0 ng/mL. CONCLUSION: Clonidine-stimulated growth hormone concentrations ≥3 ng/mL, as measured by immunochemiluminescent assay, suggest responsiveness to the stimulus regardless of gender, body mass index standard deviation score or pubertal stage.


Assuntos
Agonistas de Receptores Adrenérgicos alfa 2/farmacologia , Estatura , Clonidina/farmacologia , Transtornos do Crescimento/diagnóstico , Hormônio do Crescimento/deficiência , Hormônio do Crescimento Humano/sangue , Adolescente , Estudos de Casos e Controles , Criança , Pré-Escolar , Feminino , Transtornos do Crescimento/sangue , Transtornos do Crescimento/etiologia , Hormônio do Crescimento/sangue , Humanos , Imunoensaio/métodos , Fator de Crescimento Insulin-Like I/análise , Medições Luminescentes/métodos , Masculino , Estudos Prospectivos , Curva ROC
2.
Clinics ; 71(4): 226-231, Apr. 2016. tab, graf
Artigo em Inglês | LILACS | ID: lil-781421

RESUMO

OBJECTIVES: To establish cut-off values for growth hormone concentrations using clonidine as a secretagogue and an immunochemiluminescent assay as the method of measurement and to analyze the response time as well as the influence of gender, nutritional status and pubertal stage. METHODS: A total of 225 tests were performed in 3 patient groups, categorized as group 1 (normal), group 2 (idiopathic short stature) and group 3 (growth hormone deficiency). Among the 199 disease-free individuals, 138 were prepubertal, and 61 were pubertal. Clonidine (0.1 mg/m2) was orally administered, and the growth hormone level was measured by immunochemiluminescent assay. The growth hormone peak and the difference between the growth hormone peak and the baseline level were then analyzed. Statistical analyses were performed using Student’s t-test or the Mann-Whitney test and Kruskal-Wallis test followed by Dunn’s post hoc test. Cut-off values were determined using a receiver operating characteristic curve. RESULTS: Group 1 and group 2 had no difference in growth hormone peak, gender, body mass index standard deviation score, or pubertal stage. Group 3 exhibited a significantly lower growth hormone peak than the other groups did. The receiver operating characteristic curve demonstrated that growth hormone concentrations ≥ 3.0 ng/mL defined responsiveness to clonidine. In total, 3.02% of individuals in group 1 and group 2 were considered false positive, i.e., these children lacked growth hormone deficiency and had a peak below 3.0 ng/mL. CONCLUSION: Clonidine-stimulated growth hormone concentrations ≥3 ng/mL, as measured by immunochemiluminescent assay, suggest responsiveness to the stimulus regardless of gender, body mass index standard deviation score or pubertal stage.


Assuntos
Humanos , Masculino , Feminino , Pré-Escolar , Criança , Adolescente , Agonistas de Receptores Adrenérgicos alfa 2/farmacologia , Estatura , Clonidina/farmacologia , Transtornos do Crescimento/diagnóstico , Hormônio do Crescimento/deficiência , Hormônio do Crescimento Humano/sangue , Estudos de Casos e Controles , Transtornos do Crescimento/sangue , Transtornos do Crescimento/etiologia , Hormônio do Crescimento/sangue , Imunoensaio/métodos , Fator de Crescimento Insulin-Like I/análise , Medições Luminescentes/métodos , Estudos Prospectivos , Curva ROC
3.
ACM arq. catarin. med ; 41(3)jul.-set. 2012. ilus
Artigo em Português | LILACS | ID: lil-664827

RESUMO

A Síndrome de Turner (ST) é uma doença genéticacaracterizada pela monossomia completa ou parcial docromossomo X e possui uma grande variabilidade fenotípica,podendo se manifestar na forma clássica oucom poucos sinais dismórficos que possam chamaratenção ao diagnóstico. Mulheres com Síndrome deTurner têm um risco cardiovascular duas vezes maiorque a população geral e apresentam maior prevalênciade hipertensão arterial sistêmica, dislipidemia, aumentoda resistência insulínica e deficiência estrogênica,além de doenças cardíacas congênitas, principalmenteacometendo grandes vasos, podendo estar presenteem até 50% das mulheres com ST. Devido a essas complicaçõescardiovasculares, o reconhecimento de possíveismanifestações cardíacas agudas em pacientescom anomalias genéticas torna-se imprescindível parao sucesso terapêutico. O objetivo do presente artigo édescrever um caso de infarto agudo do miocárdio emuma paciente jovem com Síndrome de Turner.


Turner?s syndrome is a genetic disease related eitherto a homogeneous complete or a partial XO monosomyand has a fenotipic variability, presenting suchin a classic syndrome or with few dysmorfic signs thatcan draw attention to diagnosis. Womem with Turner?ssyndrome have a cardiovascular risk twice higher thangeneral population and presents more prevalence inhypertension, dyslipidemia, insulin resistence and estrogendeficiency, besides cardiac congenital cardiacdiseases, mainly affecting big vassels, in approximately50% of these patients. Due to these cardiovascularcomplications, recognition of possible acute cardiacmanifestations in patients with genetic abnormalities isnecessary to therapeutic success. The goal of this articleis to present a case report of a young woman with AMIand Turner syndrome.

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